Effect of copper on extracellular levels of key pro-inflammatory molecules in hypothalamic GN11 and primary neurons

Copper dyshomeostasis is responsible for the neurological symptoms observed in the genetically inherited copper-dependent disorders (e.g., Menkes’ and Wilson's diseases), but it has been also shown to have an important role in neurodegenerative diseases such as Alzheimer disease, prion diseases...

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Veröffentlicht in:	Neurotoxicology (Park Forest South) 2009-07, Vol.30 (4), p.605-612
Hauptverfasser:	Spisni, Enzo, Valerii, Maria Chiara, Manerba, Marcella, Strillacci, Antonio, Polazzi, Elisabetta, Mattia, Toni, Griffoni, Cristiana, Tomasi, Vittorio
Format:	Artikel
Sprache:	eng
Schlagworte:	Acute-Phase Proteins - metabolism Analysis of Variance Animals Animals, Newborn Biological and medical sciences Cells, Cultured Cerebral Cortex - cytology Chemical and industrial products toxicology. Toxic occupational diseases Copper Copper - metabolism Copper - pharmacology Culture Media, Conditioned - chemistry Cyclophilin A Cyclophilin A - metabolism Cytokines - metabolism Dose-Response Relationship, Drug Extracellular Fluid - drug effects Extracellular Fluid - metabolism Hypothalamus - cytology Inflammation Lipocalins - metabolism Medical sciences Metals and various inorganic compounds Mice Neurons - drug effects Neutrophil gelatinase-associated lipocalin (NGAL) Osteonectin - metabolism Peptide Mapping Proto-Oncogene Proteins - metabolism Rats Rats, Wistar Secreted protein acidic and rich in cysteine (SPARC) Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization - methods Spectrophotometry, Atomic Toxicology Trace Elements - metabolism Trace Elements - pharmacology
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